Organophosphate poisoning drug of choice?

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Organophosphate poisoning causes a buildup of acetylcholine at both muscarinic and nicotinic receptors by irreversibly inhibiting acetylcholinesterase. The most immediate, life-threatening effects are muscarinic in nature—excess secretions, bronchorrhea, bronchospasm, bradycardia, and miosis—so the first-line intervention is atropine. Atropine blocks muscarinic receptors, rapidly reducing secretions and airway constriction, and improving ventilation and hemodynamics, making it the drug of choice for initial management.

Pralidoxime works differently: it reactivates acetylcholinesterase by cleaving the organophosphate from the enzyme, which helps reverse both muscarinic and especially nicotinic effects like muscle weakness and paralysis. Its benefit is greatest when given early and typically in conjunction with atropine after initial stabilization. Activated charcoal may be helpful if ingestion was recent to limit absorption, but it does not address the acute cholinergic crisis directly. Diazepam can be used for seizures or agitation as needed, but again, it does not treat the cholinergic excess by itself.